J Cancer 2021; 12(16):4933-4944. doi:10.7150/jca.57152

Research Paper

MicroRNA-124-3p inhibited progression of nasopharyngeal carcinoma by interaction with PCDH8 and the inactivation of PI3K/AKT/mTOR pathway

Jiacai Ye1,2, Quanxing Liao4, Xiaohui Zeng3, Chang Liu4, Yan Ding2, Xuefeng Liu3, Lisi Zeng3✉*, Tianpei Guan4✉*, Yawei Yuan1,2✉*

1. Department of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
2. Department of Radiation Oncology, Affiliated Cancer Hospital and Institute of Guangzhou Medical University, Guangzhou, China.
3. Institute of Oncology, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou, China.
4. Department of Abdominal Surgery (Section 2), Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou, China.
* These authors jointly supervised this work.

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Citation:
Ye J, Liao Q, Zeng X, Liu C, Ding Y, Liu X, Zeng L, Guan T, Yuan Y. MicroRNA-124-3p inhibited progression of nasopharyngeal carcinoma by interaction with PCDH8 and the inactivation of PI3K/AKT/mTOR pathway. J Cancer 2021; 12(16):4933-4944. doi:10.7150/jca.57152. Available from https://www.jcancer.org/v12p4933.htm

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Abstract

Nasopharyngeal carcinoma (NPC) is characterised by distinct geographical distribution and is particularly prevalent in Asian countries. But the mechanisms related to the progression of nasopharyngeal carcinoma (NPC) are not completely understood. MiR-124-3p functions as a tumor suppressor in many kinds of human cancers. Here, we explored the effects and mechanism of miR-124-3p on the proliferation and colony formation in NPC. In our study, we reported that miR-124-3p was significantly downregulated in NPC tissues and cell lines. Overexpression miR-124-3p decreased NPC cell proliferation and colony formation abilities. Meanwhile, knockdown miR-124-3p increased proliferation and colony formation abilities. Additionally, dual-luciferase assay showed that miR-124-3p could positively regulated PCDH8 by targeting its 3'-UTR. Overexpression of PCDH8 could partially rescue the proliferation and colony formation role of miR-124-3p inhibitor. Our study indicated that miR-124-3p played a tumor suppressor by directly interacting with PCDH8 and inhibiting the activation of the phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling pathway. Overall, we found that miR-124-3p inhibited the activation of the PI3K/AKT/mTOR signaling pathway in NPC by interacting with PCDH8. Thus, PCDH8 may be a potential molecular target that impeded NPC proliferation and colony formation.

Keywords: MicroRNA-124-3p, tumor proliferation, growth, nasopharyngeal carcinoma, protocadherin-8, phosphatidylinositol 3-kinase/AKT/mammalian target of rapamycin